While the University is defending itself, can’t we all agree to stop this kind of research?

Research at Boston University that involved testing a lab-made hybrid version of the SARS-CoV-2 virus is garnering heated headlines alleging the scientists involved could have unleashed a new pathogen.

There is no evidence the work, performed under biosecurity level 3 precautions in BU’s National Emerging Infectious Diseases Laboratories, was conducted improperly or unsafely.

In fact, it was approved by an internal biosafety review committee and Boston’s Public Health Commission, the university said Monday night.

But it has become apparent that the research team did not clear the work with the National Institute of Allergy and Infectious Diseases, which was one of the funders of the project.

The agency indicated it is going to be looking for some answers as to why it first learned of the work through media reports.

Emily Erbelding, director of NIAID’s division of microbiology and infectious diseases, said the BU team’s original grant applications did not specify that the scientists wanted to do this precise work.

Nor did the group make clear that it was doing experiments that might involve enhancing a pathogen of pandemic potential in the progress reports it provided to NIAID.

The University also noted that the research was reviewed and approved by the Institutional Biosafety Committee (IBC), which consists of scientists as well as local community members, and that the Boston Public Health Commission had approved the research.

“They’ve sensationalized the message, they misrepresent the study and its goals in its entirety,” says Ronald B. Corley, NEIDL director and BU Chobanian & Avedisian School of Medicine chair of microbiology, of the news reports.

The study set out to examine the spike proteins on the SARS-CoV-2 Omicron variant (BA.1). Researchers were interested in comparing the variant with the original virus strain, known as the Washington strain.

They wanted to find out if the virus was truly less virulent, says Corley, “simply because it wasn’t infecting the same cells as the initial strain.” They were “interested in what part of the virus dictates how serious of a disease a person will get.”